Abstract: Ferroptosis, a form of non-apoptotic cell death, mainly depends on iron and reactive oxygen species (ROS) to trigger oxidative-reduction imbalance, causing membrane lipid peroxidation, cell membrane damage, and subsequent cell death. Recently, its crucial roles in embryonic development, metabolic regulation, neurodegenerative diseases, and cancer therapy have been unveiled. This article delves into the dynamic balance of cell membrane lipid peroxidation injury and repair mechanisms during ferroptosis, and dissects the multifaceted functions of mitochondria, lysosomes, etc., in regulating ferroptosis. The imbalance between membrane damage and repair is a hallmark of ferroptosis. The antioxidant system maintains membrane integrity by regulating lipid metabolism and redox homeostasis, while membrane repair mechanisms prevent cell death by removing lipid peroxides. Moreover, organelles interact dynamically through iron metabolism, ROS signaling, and lipid peroxide diffusion, modulating ferroptosis sensitivity. This article encapsulates the latest progress in ferroptosis mechanisms and highlights the potential of targeting membrane repair and organelle interactions for disease therapy, offering novel insights for precise disease intervention.